Rhinitis is a term describing the symptoms produced by nasal irritation or inflammation. Symptoms of rhinitis include runny nose, itching, sneezing and stuffy nose due to blockage or congestion. These symptoms are the nose's natural response to inflammation and irritation, and they are often associated with itching of the eyes.
The nose normally produces mucus, which traps substances like dust, pollen, pollution, and germs such as bacteria and viruses. Mucus flows from the front of the nose and drains down the back of the throat. When mucus production is excessive, it can flow from the front, as a runny nose, or become noticeable from the back, as post-nasal drip. Nasal mucus, normally a thin, clear liquid, can become thick or colored, perhaps due to dryness, infection or pollution. When post-nasal drip is excessive, thick, or contains irritating substances, cough is the natural response for clearing the throat.
Itching and sneezing are also natural responses to irritation caused by allergic reactions, chemical exposures including cigarette smoke, or temperature changes, infections and other factors.
The nasal tissues congest and decongest periodically. In most people, nasal congestion switches back and forth from side to side of the nose in a cycle several hours long. Some people, especially those with narrow nasal passages, notice this nasal cycle more than others. Severe congestion can result in facial pressure and pain, as well as dark circles under the eyes.
The three most common types of rhinitis are allergic, infectious, and non-allergic. Infectious rhinitis (colds or flu) are typically caused by viruses; its duration is often 3 to 7 days, and sometimes longer. Colds usually begin with a sensation of congestion, rapidly followed by runny nose and sneezing. Over the next few days, congestion becomes more prominent, the nasal mucus may become colored, and there may be a slight fever and cough. Cold symptoms resolve within a couple of weeks, although a cough may sometimes persist. Cold symptoms that last longer may be due to other causes, such as chronic rhinitis or sinusitis.
Non-allergic rhinitis refers to rhinitis having symptoms not caused by infection or allergy. Non-allergic rhinitis includes vasomotor rhinitis and irritant rhinitis. Many people have recurrent or chronic nasal congestion, excess mucus production, itching, and other nasal symptoms similar to those of allergic rhinitis, but the disorder is not caused by allergy. Irritants that can trigger vasomotor rhinitis include cigarette smoke, strong odors and fumes including perfume, hair spray, cosmetics, laundry detergents, cleaning solutions, pool chlorine, car exhaust and other air pollution. Other irritants are spices used in cooking, alcoholic beverages (particularly beer and wine), aspirin, and certain blood pressure medications. Some people are very sensitive to abrupt changes in weather or temperature. Skiers often develop a runny nose, but in some people any cold exposure may cause a runny nose. Others start sneezing when leaving a cold, air conditioned room. The duration of symptoms of non-allergic rhinitis can be perennial and/or following exposure.
Allergic rhinitis, also known as hay fever, is often caused by dust mites, animals, pollens, molds, and food. Allergic rhinitis is an inflammatory state characterized by numerous symptoms such as nasal congestion, nasal discharge, post-nasal drip, sore throat, sneezing, headache, itching of the nose and throat, facial pressure and pain, and general malaise. Settipane et al (Ann. Allergy Asthma Immunol. 86:494-508 (2001)) report that allergic rhinitis is about 3 times more prevalent than pure nonallergic rhinitis; however, a mixed picture of the two is quite common: it is estimated that 44% to 87% of patients with rhinitis have some component of mixed rhinitis.
Perennial allergic rhinitis (PAR) is the most common type of allergic rhinitis, and is typically caused by exposure to allergens such as mold spores, dust mites, animal dander and others, and can occur at any time of year. This is generally viewed as a chronic disease. Seasonal allergic rhinitis, also known as hay fever, is a reaction to pollen or mold and typically occurs during certain seasons, for example during “rag weed season” in certain locals. The duration of the allergic reactions can be several days to a few months. Occupational allergic rhinitis is similar to PAR, but it is triggered by a response to airborne allergens at work. Infectious allergic rhinitis occurs during an upper respiratory infection, such as during the common cold, in which the infecting organism releases inflammatory mediators that trigger an allergic response. Symptoms last throughout the time of infection and are often associated with an increase in sinus and bronchial infections. Hormonal allergic rhinitis occurs typically during pregnancy or in patients with other hormonal imbalances such as hypothyroidism. Idiopathic allergic rhinitis is a term used to describe allergic rhinitis in which either the allergen is not known or the cause of the inflammatory rhinitis symptoms is best defined as perennial non-allergic.
Allergic rhinitis clinically presents as some or all of the following symptoms: rhinorrhea, sneezing, nasal congestion, itching of the nose and palate, and ocular symptoms (itchy, watery eyes). (Skoner D P. Allergic rhinitis: definition, epidemiology, pathophysiology, detection, and diagnosis. J Allergy Clin Immunol 2001; 108 (1 Suppl): S2-S8)
There is a close correlation between inflammatory mediators in nasal secretions and symptoms of Allergic Rhinitis. (Lebel B, Bousquet J, Morel A, et al. Correlation between symptoms and the threshold for release of mediators in nasal secretions during nasal challenge with grass-pollen grains. J Allergy Clin Immunol 1988; 82(5 Pt 1):869-877)
Cytokines and chemokines, such as interleukin (IL)-8, as well as the mediators released by the early-phase reaction, help recruit and activate inflammatory cells, such as eosinophils, which themselves release mediators. (White M. Mediators of inflammation and the inflammatory process. J Allergy Clin Immunol 1999; 103(3 Pt 2):S378-S381)
Symptoms are therefore perpetuated, with persistent allergic rhinitis sufferers existing in a continual state of eosinophilia and increased mediator release. (Wang D Y, Clement P. Pathogenic mechanisms underlying the clinical symptoms of allergic rhinitis. Am J Rhinol 2000; 14:325-333)
Eosinophils express various membrane molecules, including FcεRI. (Capron, M., Soussi Gounni, A., Morita, M., Truong, M. J., Prin, L., Kinet, J. P. Capron, A. Eosinophils: from low- to high-affinity immunoglobulin E receptors. Allergy 1995, 50 (25 Suppl):20-23.)
Binding of the allergen-IgE complex with FcεRI on the eosinophil surface results in signal transduction, which activates the cell to release preformed, granule-associated proteins, arachidonic acid-derived products, cytokines and oxygen free radicals. (Capron, M., Desreumaux, P. Immunobiology of eosinophils in allergy and inflammation. Res Immunol 1997, 148:29-33)
A significant eosinophil activation may occur also in the very early events characterizing the reaction to allergen exposure. (Sihra, B. S., Kon, O. M., Grant, J. A., Kay, A. B. Expression of high-affinity IgE receptors (Fc epsilon RI) on peripheral blood basophils, monocytes and eosinophils in atopic and nonatopic subjects: relationship to total serum IgE concentrations. J Allergy Clin Immunol 1997, 99:699-706.)
In addition to mast cells and eosinophils, epithelial cells are also activated after allergen challenge. [Ciprandi, G., Pronzato, C., Ricca, V., Passalacqua, G., Bagnasco, M., Canonica, G. W. Allergen-specific challenge induces intercellular adhesion molecule 1 (ICAM-1 or CD54) on nasal epithelial cells in allergic subjects. Relationships with early and late inflammatory phenomena. Am J Respir Crit Care Med 1994, 150:1653-1659. Vignola, A. M., Campbell, A. M., Lacoste, P., Michel, F. B., Godard, P., Bousquet, J. Activation by histamine of bronchial epithelial cells from non asthmatic subjects. Am J Respir Cell Mol Biol 1993, 9:411-417.
Allergic rhinitis and asthma are closely-related entities influenced by common pathogenetic processes, linked by similar physiologic characteristics, sustained and amplified by interconnected mechanisms in atopic individuals. A recent clinical study has shown close correlations between bronchial reactivity and eosinophil percentages in nasal brushing, ‘at baseline’ and after nasal allergen challenge. (Silvestri M, Battistini E, Defilippi A-C, Sabatini F., Sale R, Pecora S, and Rossi G A. J Invest Allergol Clin Immunol 2005; Vol. 15(4): 266-276)
Allergic rhinitis is an inflammatory reaction, where a high degree of cell-to-cell communication is needed to orchestrate this inflammatory immune response. A variety of cytokines and adhesion receptors play an important role in the allergic late phase reaction. (C. Bachert, U. Hauser, B. Prem, C. Rudack and U. Ganzer. Proinflammatory cytokines in allergic rhinitis. European Archives of Oto-Rhino-Laryngology Volume 252, Supplement 1/January, 1995)
Sinusitis (rhinosinusitis) is inflammation or infection of any of the four groups of sinus cavities in the skull, which open into the nasal passages. Sinusitis is not the same as rhinitis, although the two may be associated and some of their symptoms may be similar. Sinusitis affects approximately 16% of U.S. adults. Viral upper respiratory tract infections and allergic rhinitis, which affects up to 35.9 million Americans each year, are the two most common predisposing conditions for sinusitis. Medical treatments that are useful in treating recurrent acute and chronic sinusitis include the same range of medications as used for rhinitis, such as intranasal corticosteroids and decongestants. A course of oral antibiotics may be indicated for sinusitis.
Coexisting sources of nasal inflammation can manifest themselves with similar symptoms and can participate in the diffuse problem of sinusitis. There is histopathologic evidence that rhinitis was associated with chronic sinusitis. Several of the consensus documents mentioned above, most recently that published simultaneously in the Journal of Allergy and Clinical Immunology and Otolaryngology—Head and Neck Surgery in December 2004, officially adopted the term rhinosinusitis in preference to sinusitis. (Rhinosinitis and the revised “Sinusitis practice parameters”. Hamilos D L et al. J Allergy and Clin Immunol. December 2005)
Rhamnolipids are naturally occurring biosurfactants constructed of rhamnose sugar molecules and β-hydroxyalkanoic acids. Production of rhamnose containing glycolipids was first described in Pseudomonas aeruginosa by Jarvis and Johnson. (Jarvis, F. G. and Johnson, M. J., A glycolipid produced by Pseudomonas aeruginosa. J. Am. Oil Chem. Soc., 1949, 71, 4124-4126.)
L-Rhamnosyl-L-rhamnosyl-β-hydroxydecanoyl-β-hydroxydecanoate and L-rhamnosyl-β-hydroxydecanoyl-β-hydrocydecanoate, are the principal glycolipids produced by P. aeruginosa. (Edward, J. R. and Hayashi, J. A., Structure of rhamnolipid from Pseudomonas aeruginosa. Arch. Biochem. Biophys., 1965, 111, 415-421.)
Rhamnolipids have demonstrated low irritancy and even anti-irritating effects when used topically on the skin. (Stipcevic T, et al. J Dermatol Sci. 2005 November; 40(2): 141-143.)
U.S. Pat. No. 7,261,171 discloses the use of rhamnolipids in re-epithelization of skin, particularly in wound healing with the diminution of fibrosis.
U.S. Pat. No. 5,514,661 discloses the use of rhamnolipids for treating autoimmune diseases of organ specific and organ non-specific autoimmune diseases, AIDS, Parkinson's disease, Alzheimer's disease and amyotrophic lateral sclerosis.
There is a need for improved methods for treating rhinitis and sinusitis. The method should be safe, effective and have no significant side effects.